POS1322 LOW CD32 EXPRESSION ACCOUNTS FOR THE ASSOCIATION OF CD21LOW B CELLS WITH DIGITAL ULCERS IN SYSTEMIC SCLEROSIS
Authors: E. Kourkouni, A. Mavropoulos, S. Tsiogkas, T. Simopoulou, C. Katsiari, D. Bogdanos, L. Sakkas
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Abberations of B cells have been implicated in the pathogenesis of systemic sclerosis(SSc) [1] and CD21<sup>low</sup> B cells, which express high levels of activation markers, have recently been associated with vascular manifestations in SSc [2]. CD32 (FcγRII), comprised of three isoforms A, B and C, is involved in B cell regulation and antibody production. B cells do not express FcγRIIA and mainly express the inhibitory FcγRIIB isoform [3]. <h3>Objectives</h3> The aim of our study was to assess the expression of CD32 in CD21<sup>low</sup> B cells in SSc patients with digital ulcers (DUs). <h3>Methods</h3> Thirty patients, 23 women (median age 56 years. Interquartile range 32 -81) and 7 men (median age 60 years, Interquartile range 52-79) fulfilling the ACR/EULAR 2013 criteria for SSc were included in the study. Peripheral blood mononuclear cells from patients were analyzed with multicolor flow cytometry using anti-CD19 monoclonal antibody (moAb), anti-CD21 moAb, and anti-CD32 moAb, that recognizes both the FcγRIIA and FcγRIIB isoforms. <h3>Results</h3> The percentage of CD21<sup>low</sup> B cells was significantly increased in patients with DUs compared to patients without DUs (difference between means: 24.6, 95% CI 5.37-43.8, p = 0.014). The percentage of CD21<sup>low</sup>CD32<sup>low</sup> B cells were significantly increased in patients with DUs compared to patients without DUs (difference between means: 23.24 ± 7.364, 95% CI 8.152-38.32, p = 0.0038) (Figure1A). The percentage of CD21<sup>low</sup>CD32<sup>high</sup> B cells was significantly decreased in the DUs group (difference between means: -26.61 ± 9.312, 95% CI -45.69 to -7.539, p = 0.0080) (Figure 1B). <h3>Conclusion</h3> Our study suggests that low expression of CD32 accounts for the association of CD21<sup>low</sup> B cells with DUs in SSc and implies that CD32 may have an inhibitory effect on CD21<sup>low</sup> B cells. <h3>References</h3> [1]Sakkas LI et al.The role of B cells in the pathogenesis of systemic sclerosis: An update. Rheumatology 2022; Oct 11:keac578. [2]Marrapodi R et al. CD21low B cells in systemic sclerosis:A possible marker of vascular complications. Clin Immunol 2020; 213;108:364 [3]Annania JC et al. The human FcvRII(CD32) family of leukocyte FcR in health and disease. Front Immunol 2019; 10:464 <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> Evangelia Kourkouni: None declared, ATHANASIOS MAVROPOULOS: None declared, Sotirios Tsiogkas: None declared, Theodora Simopoulou Speakers bureau: Abbvie, Boehringer Ingelheim, Pfizer, Grant/research support from: Grants to support the research and educational activities from Genesis pharma. Travel bursaries to attend scientific meetings and congresses from Amgen, Janssen, Christina Katsiari Speakers bureau: Speaker fees from Boehrimger, Roche, Abbvie, UCB, Lilly, Bristol, Novartis, GlaxoSmithKlime, Consultant of: Comsultant fees from Mylan, Grant/research support from: Grants to support the research and educational activities as well as travel bursaries to attend scientific meetings and congresses from Amgen, Boehrimger, Roche, Abbvie, UCB, Lilly, Bristol, Novartis, GlaxoSmithKlime, Celltrion Healthcare, Dimitrios Bogdanos Speakers bureau: Enorasis, Genesis Pharma, Novartis, Euroimmun, Menarini Hellas, Boehringer Ingelheim, Fresenius Kabi, Werfen Diagnosticsw, Grant/research support from: Grants to support the research and educational activities of his Department from Elpen, Boehringer Ingelheim, Demo and Menarini Hellas. Received travel bursaries to attend scientific meetings and congresses from Hospital Line, Pfizer, Elpen, Aenorasis Hellas, Novartis and IFT Hellas, Lazaros Sakkas: None declared.